Inhibition of glutathione synthesis of Ascaris suum by buthionine sulfoximine

1996 ◽  
Vol 82 (4) ◽  
pp. 372-374 ◽  
Author(s):  
A. S. Hussein ◽  
R. D. Walter
Keyword(s):  
Ascaris Suum ◽  
Buthionine Sulfoximine ◽  
Glutathione Synthesis

Interactions of nitroglycerin and sulfhydryl-donating compounds in coronary microvessels

1994 ◽  
Vol 266 (1) ◽  
pp. H291-H297 ◽  
Author(s):  
R. M. Wheatley ◽  
S. P. Dockery ◽  
M. A. Kurz ◽  
H. S. Sayegh ◽  
D. G. Harrison
Keyword(s):  
Redox Potential ◽  
Potent Inhibitor ◽  
Buthionine Sulfoximine ◽  
Glutathione Synthesis ◽  
Endothelin 1 ◽  
Intracellular Glutathione ◽  
Enzymatic Bioconversion

Previous studies have shown the effect of nitroglycerin on coronary microvessels < 100 microns in diameter is markedly enhanced by L-cysteine. These studies were performed to examine the mechanisms responsible for this effect. Under control conditions, nitroglycerin caused potent dilations of large (> 200 microns diam) coronary microvessels while having minimal effects on small (< 100 microns diam) coronary microvessels [peak relaxations 85 +/- 4 vs. 23 +/- 3% (mean +/- SE) of endothelin-1-constricted vessels, respectively]. L-Cysteine (100 microM) and N-acetylcysteine (100 microM) markedly enhanced nitroglycerin-induced relaxations of small coronary microvessels (peak relaxation 84 +/- 6 and 87 +/- 12%, respectively) while having no effect on relaxations of vessels > 100 microns. In contrast, neither L-methionine (100 microM) nor glutathione (100 microM) enhanced nitroglycerin's vasodilation of small coronary microvessels. The effects of L-cysteine and N-acetylcysteine on the augmentation of nitroglycerin vasodilatation in smaller coronary microvessels was abolished in the presence of buthionine sulfoximine (100 microM), a potent inhibitor of intracellular glutathione synthesis. Buthionine sulfoximine had no effect on the vasodilatation produced by nitroprusside. These data demonstrate that, in smaller coronary microvessels, L-cysteine and N-acetylcysteine enhance nitroglycerin-induced vasodilatation by increasing intracellular glutathione concentrations. Intracellular glutathione, formed from either L-cysteine or N-acetylcysteine, may participate in the formation of an intermediate of nitroglycerin biotransformation or may maintain a redox potential within coronary microvessels that favors enzymatic bioconversion of nitroglycerin.

Glutathione modulates toxic oxygen metabolite injury of canine chief cell monolayers in primary culture

1988 ◽  
Vol 254 (1) ◽  
pp. G49-G56 ◽  
Author(s):  
C. E. Olson
Keyword(s):  
Oxidant Stress ◽  
Buthionine Sulfoximine ◽  
Cell Lysis ◽  
Glutathione Depletion ◽  
Glutathione Synthesis ◽  
Chief Cells ◽  
Cell Monolayers ◽  
Lactate Dehydrogenase Release ◽  
Endogenous Antioxidant ◽  
Generating System

Cultured canine gastric chief cells exposed to a toxic oxygen metabolite-generating system (xanthine plus xanthine oxidase) demonstrated minimal cytolysis, suggesting that these cells have important endogenous antioxidant mechanisms. We have quantified the role of glutathione for protection against toxic oxygen metabolites by measuring cell lysis by lactate dehydrogenase release after variable depletion and repletion of cellular glutathione content. In the absence of exogenous oxidant stress, the glutathione content of chief cells can be depleted to less than 0.2 nmol total glutathione/micrograms DNA or 22% of control without cell lysis over 5 h. However, when challenged with the oxygen metabolite-generating system, cytolysis was greatly enhanced by glutathione depletion. Oxygen metabolite-mediated cytolysis after glutathione depletion was inhibited by exogenous catalase, thiourea, and deferoximine, but not superoxide dismutase or mannitol. These data suggested that hydrogen peroxide and hydroxyl radical mediated cytolysis in glutathione-depleted chief cells. If a substrate for glutathione synthesis, N-acetyl-L-cysteine, was provided to the depleted cells for 1 h before challenge with the oxygen radical-generating system, cell lysis was markedly decreased. However, if glutathione synthesis was blocked during the repletion period by buthionine sulfoximine, protection was not restored. The data supported an important role for glutathione as an endogenous antioxidant, which modulated the sensitivity of cultured chief cells to toxic oxygen metabolite injury.

scholarly journals Effect of inhibition of glutathione synthesis on insulin action: in vivo and in vitro studies using buthionine sulfoximine

2000 ◽  
Vol 349 (2) ◽  
pp. 579 ◽  
Author(s):  
Mogher KHAMAISI ◽  
Oren KAVEL ◽  
Moti ROSENSTOCK ◽  
Michal PORAT ◽  
Michal YULI ◽  
...  
Keyword(s):  
Insulin Action ◽  
Buthionine Sulfoximine ◽  
In Vitro Studies ◽  
Glutathione Synthesis
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